forms had somewhat similar structures and antiox-idant activities, they differed in their abilities to prevent or reverse specific vitamin E deficiency symptoms (e.g., fetal resorption, muscular dystrophy, and encephalomalacia). a-Tocopherol with three methyl groups and a free hydroxyl group on the chromanol ring with the phytyl tail meeting the ring in the R-orientation (Figure 1) had the highest biological activity. This specific structural requirement for biological, but not chemical, activity is now known to be dependent upon the hepatic a-tocopherol transfer protein (a-TTP), as discussed below. a-TTP maintains plasma and, indirectly, tissue a-tocopherol concentrations.

Molecular Function

In addition to antioxidant activity, there are specific a-tocopherol-dependent functions that normalize cellular functions in a variety of cells. a-Tocopherol plays a critical role through its ability to inhibit the activity of protein kinase C, a central player in many signal transduction pathways. Specifically, it modulates pathways of platelet aggregation, endothelial cell nitric oxide production, monocyte/macrophage superoxide production, and smooth muscle cell proliferation. Regulation of adhesion molecule expression and inflammatory cell cytokine production by a-tocopherol has also been reported. However, most of the information in this area has been obtained from in vitro studies. More studies in humans are needed to relate a-tocopherol intakes and tissue concentrations to optimal tissue responses.

Vitamin E metabolism a- and 7-tocopherols, as well as a-and 7-tocotrienols, are metabolized to a- and 7-CEHCs (2,5,7,8-tetra-methyl- and 2,7,8-trimethyl-2-(2' carboxyethyl)-6-hydroxychromans), respectively. About 1% of a dose of a-tocopherol or tocotrienol, or 5% of a dose of 7-tocopherol or tocotrienol is excreted in the urine as CEHCs. The importance of vitamin E metabolism in the regulation of vitamin E status is unknown.

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